This classification scheme is more acceptable because it takes into consideration the beta-lactamase inhibitors and beta lactam substrates that are clinically relevant (5). Beta-lactamases with carbapenemase activity are a cause for concern and include serine oxacillinase and metallo-beta-lactamase, which are classified as Ambler Class D and Ambler Class B types, respectively. OXA type carbapenemase, which is able to hydrolyze carbapenem and was first studied from a clinical isolate of A. baumannii, has been found to be plasmid encoded and transferable.

It was named blaOXA-23 and is now studied extensively because it contributes to carbapenem resistance in A. baumannii Alpelisib in vivo (6). The blaOXA-23 gene cluster has two other enzymes that are closely related, blaOXA-27 and blaOXA-49. In addition, two more gene clusters contributing to resistance

that include blaOXA-24-like and blaOXA-58-like have been reported. The natural presence of blaOXA-51-like genes has been observed to be intrinsic to A. baumanni and is chromosomally encoded; hence this is used as an identification AG-014699 ic50 marker of this species (7). Rapid acquisition of resistance to meropenem and other carbapenems poses an issue in the treatment of A. baumannii infections. In a report presented in 2007, over 25% of A. baumannii isolates were recorded to be carbapenem resistant (8). In a tertiary care hospital in North India, meropenem resistance was reported in 6.4% of Acinetobacter Protirelin spp. tested (9). In India, several workers have reported metallo-beta-lactamases resulting in resistance in A. baumannii to be prevalent (10, 11). These findings are a pointer to the threat posed by the treatment of carbapenem resistant Acinetobacter in India. The presence of the insertion sequence ISAba1 upstream of the OXA carbapenemase gene has been identified as a key factor affecting over expression of these genes (1). The prevalence of OXA-type genes and their association with ISAba1 in Acinetobacter from India is not well understood. Persistence in the hospital environment is an important characteristic of Acinetobacter spp. It is suspected that the ability to adhere to surfaces

and form biofilm both helps the organism to persist in the environment and also plays a role in its virulence (1, 12). However, there is very little information on the ability of clinical isolates to form biofilm. Though a number of molecular typing methods have been used as epidemiological tools, they have generally been applied to investigate outbreaks (1). Therefore, in this study, non-outbreak associated clinical isolates of Acinetobacter from four hospitals were studied for the presence of OXA-type β-lactamase genes and ISAba1 upstream of these genes, their resistance to meropenem and their biofilm forming ability. Diversity among the strains was assessed by fingerprinting the isolates using RAPD. Sixty two isolates of Acinetobacter spp.